癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
ATG4D antibody (Ascites)
Mouse Monoclonal Antibody (Mab)
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- 实验流程
- 背景知识
Application 
| WB, E |
|---|---|
| Primary Accession | Q86TL0 |
| Other Accession | NP_116274.3 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Isotype | IgG1,K |
| Clone Names | 222CT15.4.1 |
| Calculated MW | 52922 Da |
| Gene ID | 84971 |
|---|---|
| Other Names | Cysteine protease ATG4D, 3422-, AUT-like 4 cysteine endopeptidase, Autophagin-4, Autophagy-related cysteine endopeptidase 4, Autophagy-related protein 4 homolog D, Cysteine protease ATG4D, mitochondrial, ATG4D, APG4D, AUTL4 |
| Target/Specificity | This ATG4D monoclonal antibody is generated from mouse immunized with ATG4D recombinant protein. |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Mouse monoclonal antibody supplied in crude ascites with 0.09% (W/V) sodium azide. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | ATG4D antibody (Ascites) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | ATG4D {ECO:0000303|PubMed:19549685, ECO:0000312|HGNC:HGNC:20789} |
|---|---|
| Function | [Cysteine protease ATG4D]: Cysteine protease that plays a key role in autophagy by mediating both proteolytic activation and delipidation of ATG8 family proteins (PubMed:21177865, PubMed:29458288, PubMed:30661429). The protease activity is required for proteolytic activation of ATG8 family proteins: cleaves the C-terminal amino acid of ATG8 proteins MAP1LC3 and GABARAPL2, to reveal a C-terminal glycine (PubMed:21177865). Exposure of the glycine at the C-terminus is essential for ATG8 proteins conjugation to phosphatidylethanolamine (PE) and insertion to membranes, which is necessary for autophagy (By similarity). In addition to the protease activity, also mediates delipidation of ATG8 family proteins (PubMed:29458288, PubMed:33909989). Catalyzes delipidation of PE-conjugated forms of ATG8 proteins during macroautophagy (PubMed:29458288, PubMed:33909989). Also involved in non-canonical autophagy, a parallel pathway involving conjugation of ATG8 proteins to single membranes at endolysosomal compartments, by catalyzing delipidation of ATG8 proteins conjugated to phosphatidylserine (PS) (PubMed:33909989). ATG4D plays a role in the autophagy-mediated neuronal homeostasis in the central nervous system (By similarity). Compared to other members of the family (ATG4A, ATG4B or ATG4C), constitutes the major protein for the delipidation activity, while it promotes weak proteolytic activation of ATG8 proteins (By similarity). Involved in phagophore growth during mitophagy independently of its protease activity and of ATG8 proteins: acts by regulating ATG9A trafficking to mitochondria and promoting phagophore- endoplasmic reticulum contacts during the lipid transfer phase of mitophagy (PubMed:33773106). |
| Cellular Location | [Cysteine protease ATG4D]: Cytoplasm |
| Tissue Location | Widely expressed in testis. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Autophagy is the process by which endogenous proteins and damaged organelles are destroyed intracellularly. Autophagy is postulated to be essential for cell homeostasis and cell remodeling during differentiation, metamorphosis, non-apoptotic cell death, and aging. Reduced levels of autophagy have been described in some malignant tumors, and a role for autophagy in controlling the unregulated cell growth linked to cancer has been proposed. This gene encodes a member of the autophagin protein family. The encoded protein is also designated as a member of the C-54 family of cysteine proteases.
REFERENCES
Betin, V.M., et al. J. Cell. Sci. 122 (PT 14), 2554-2566 (2009) :
Lamesch, P., et al. Genomics 89(3):307-315(2007)
Marino, G., et al. J. Biol. Chem. 278(6):3671-3678(2003)
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